Introduction

Gestational diabetes mellitus (GDM) is carbohydrate intolerance of varied severity with first onset or first recognition during pregnancy ^[1]. GDM is one of the most prevalent medical conditions in pregnant population. Global prevalence of GDM is on the rise. A study conducted among pregnant population in south Kerala had shown a prevalence as high as11.2%.^[2]

Gestational diabetes seems to stem from the placenta and several placental hormones that help the development of fetus during pregnancy. During the second and third trimesters, these “insulin-antagonist” hormone levels increase and can cause insulin resistance. Insulin resistance makes it difficult for the mother’s body to properly utilize insulin, the hormone that manages glucose or blood sugar levels. This causes a higher-than-normal blood sugar level or hyperglycemia. Hence GDM usually develops between the 24^th and 28^th week of pregnancy.  Normally, after delivery, these hormone levels, as well as glucose levels, return to normal^[3]. According to American Diabetes Association (ADA), GDM is pathophysiologically similar to Type 2 diabetes in that the abnormality is in islets cell function or peripheral insulin resistance at receptor level. Studies suggest that the peripheral insulin resistance that characterize GDM likely results from several integrated mechanisms including a decrease in insulin receptor number, a post-receptor defect in insulin action and alterations in glucose transport systems^[4,5].

1. Metzger, B. E. and Coustan, D. R.; “Summary and Recommendations of the Fourth International Workshop Conference on Gestational Diabetes Mellitus”; Diabetes Care, Volume 21 (Supplement 2), 1998, Page(s): B161 – B 167
2. K Paulose ”Prevalence of gestational diabetes in south  Kerala” ,KMJ issue 3 october 2008, pages(s): 14 -16.
3. Ryan, E. A., O’Sullivan, M. J., and Skyler, J. S.; “Insulin Action during Pregnancy: Studies with the Euglycemic Clamp Technique”; Diabetes, Volume 34,1985, Page(s): 384 – 389.
4. Moore, P., Kolterman, O., Weyant, J., Olesfsky, J. M.; “Insulin Binding in Human Pregnancy, Comparisons to the Post Partum, Luteal and Follicular States”; Journal of Clinical Endocrinology and Metabolism, Volume 52, 1987, Page(s): 937
5. Puavilai, G., Drobny, E. C., Domont, L. A., Baumann, G.; ”Insulin Receptors and Insulin in Human Pregnancy, Evidence for a Post Receptor Defect in Insulin Action”; Journal of Clinical Endocrinology and Metabolism, Volume 54, 1982, Page(s):247
6. Norwitz, Errol R.; “Endocrine diseases of Pregnancy, Reproductive Endocrinology, Physiology, Pathophysiology and Clinical Management”
7. Thomas, M. Alyce, Gutierrez, Yolanda Monroy; “Pathophysiology of GDM”; American Diabetes Association Guide to GDM
8. Karunakaran, L; “GDM Changing Concepts”; FOG Journal Volume 4, Issue 2, October 2010
9. American Diabetes Association; “Gestational Diabetes Mellitus”; Diabetes care, Volume 27, Supplement 1, 2004
10. American Diabetes Association: GDM; Diabetes Care, Volume 27, Issue 1, 2004, Page(s): 388 – 390
11. Solomon, C. G., Willett, W. C., Carey, V. J. et al; “A Prospective Study of Pregravid Determinants of GDM”; J A M A, Volume 278, 1997, Page(s): 1078 – 1083
12. “Acta Diabetologia”; Volume 41, November 4, Page(s); 154 – 157
13. WHO fact sheet overweight and obesity, june 2016.
14. 1Hedderson, M. M., Williams, M. A., Holt, V. L., Weiss, N. S., Ferrara, A.; “BMI and Weight Gain Prior to Pregnancy and Risk of GDM”; American Medical Journal of Obstetrics and Gynaecology, Volume 198, 2008, Page(s): 409
15. Tovar, A., Mast, A., Bermudez, O. I., Hyatt, R. R., Chasan-Taber, L.; “The Impact of Gestational Weight Gain and Diet in Abnormal Glucose Tolerance during Pregnancy in Hispanic Women”; Maternal Child Health Journal, 2008
16. Ferrara, A., Kahn, H. S., Quesenberry, C., Riley, C. Heddersson, M. M.; “An Increase in Incidence of GDM Northern California”; Obstetrics and Gynaecology, Volume 103, 2004, Page(s): 526 – 533

Dr Sreekala K N

Assistant Professor, Department of Physiology, SUT AMS, TVM